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Post-concussion syndrome is symptoms that can linger following a concussion. Studies have shown cannabis reduces damage caused from brain injuries and can help patients manage the symptoms of the syndrome.
Overview of Post-Concussion Syndrome
Post-concussion syndrome (PCS) is a variety of symptoms, including headaches and dizziness, that continue for weeks and sometimes months following a concussion. A concussion is a mild traumatic brain injury that typically occurs after a direct blow to the head. Not all concussions lead to post-concussion syndrome, which doesn’t seem to be correlated to the severity of the initial blow.
What causes post-concussion symptoms to develop following certain concussions is yet to be identified. According to Mayo Clinic, some experts believe the symptoms come from structural damage to the brain or the disruption of neurotransmitter systems. Others believe that psychological factors may contribute.
In addition to headaches and dizziness, post-concussion syndrome commonly causes fatigue, irritability, anxiety, insomnia, loss of concentration and memory, and noise and light sensitivity.
Typically, symptoms associated with PCS develop within the first seven to 10 days after a concussion and eventually alleviate within a three-month period. In some cases, however, the symptoms can persist for a year or longer.
Treatment for post-concussion syndrome depends on individual symptoms. Headaches are commonly treated with medications. Time, however, is often the best therapy for treating memory and thinking problems.
Findings: Effects of Cannabis on Post-Concussion Syndrome
While research on cannabis’ direct effect on post-concussion syndrome is lacking, preclinical findings have shown that cannabis offers therapeutic benefits following brain injuries. Studies have shown that the cannabinoids found in cannabis, most specifically cannabidiol (CBD), activate the body’s cannabinoid receptors (CB1 and CB2), though evidence also suggests that the neuroprotective effects from CBD come from the cannabinoid’s activation of the 5-hydroxytriptamine1A (5-HT1A) receptor (Mishima, et al., 2005). When these receptors are activated, they provide protection against neural damage following acute and chronic brain damage (Lopez-Rodriguez, et al., 2013). For example, in one study, the administration of cannabinoids following a traumatic brain injury decreased brain swelling and inflammation and was shown to improve recovery (Shohami, et al., 2011). Another showed that CBD alone provided neuroprotection and limited brain cell death in newborn mice following a hypoxic-ischemic event (Castillo, et al., 2010). Others have showed that cannabinoids, through the activation of the endocannabinoid system, prevent glutamate excitotoxicity, intracellular calcium accumulation, activation of cell death pathways, microglia activation, neurovascular reactivity and circulating leukocytes following a brain injury. Researchers concluded that modulating the endocannabinoid system is an effective way to provide neuroprotection and prevent and reduce brain injury (Fernandez-Lopez, Lizasoain, Moro & Orgado, 2013).
Addition research has shown that cannabis’ cannabinoids provide brain and neuroprotection caused by disorders. One found that CBD reduces the oxidative stress and Alzheimer’s hallmark protein (β-amyloid), thus limiting nerve damage caused by the disorder and improving cell viability (Harvey, et al., 2012). An animal study showed that CBD and tetrahydrocannabinol (THC) treatments were effective at delaying and limiting neural damage caused by Huntington’s disease (Sagredo, et al., 2011). Another found that CBD, in addition to providing neuroprotective effects and reducing long-term brain injury, also helped restore neurobehavioral function following a hypoxia-ischemia event (Pazos, et al., 2012).
Studies have also shown that cannabis can help post-concussion syndrome patients manage the symptoms associated with the disorder. CBD can lower stress, help combat depression, improve sleep and reduce pain (Abush & Akirav, 2013) (Campos, et al., 2012) (Chagas, et al., 2013) (Russo, Guy & Robson, 2007) (Baron, 2015).
States That Have Approved Medical Marijuana for Post-Concussion Syndrome
Currently, only the state of Illinois has approved medical marijuana for the treatment of post-concussion syndrome. However, in Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment. In addition, a number of other states will consider allowing medical marijuana to be used for the treatment of post-concussion syndrome with the recommendation from a physician. These states include: California (any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), Rhode Island (other conditions subject to approval), and Washington (any “terminal or debilitating condition”).
Also, fourteen states have approved medical marijuana specifically to treat “chronic pain,” which can develop from post-concussion syndrome. These states include: Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island, Vermont and West Virginia. The states of Nevada, New Hampshire, North Dakota, Ohio and Vermont allow medical marijuana to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania, Washington and West Virginia have approved cannabis for the treatment of “intractable pain.”
Recent Studies on Cannabis’ Effect on Post-Concussion Syndrome
Abush, H., & Akirav, I. (2013). Cannabinoids Ameliorate Impairments Induced by Chronic Stress to Synaptic Plasticity and Short-Term Memory. Neuropsychopharmacology, 38(8), 1521–1534. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682147/.
Arain, M., Khan, M., Craig, L., and Nakanishi, S.T. (2015, March). Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Annals of Clinical and Translational Neurology, 2(3), 289-94. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369278/.
Baron, E.P. (2015, June). Comprehensive Review of Medicinal Marijuana, Cannabinoids, and Therapeutic Implications in Medicine and Headache: What a Long Strange Trip It’s Been… Headache, 55(6), 885-916. Retrieved from http://onlinelibrary.wiley.com/wol1/doi/10.1111/head.12570/full.
Campos, A. C., Moreira, F. A., Gomes, F. V., Del Bel, E. A., & Guimarães, F. S. (2012). Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders. Philosophical Transactions of the Royal Society B: Biological Sciences, 367(1607), 3364–3378. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481531/.
Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., and Martinez-Orgado, J. (2010). The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB2 and adenosine receptors. Neurobiology of Disease, 37, 434-440. Retrieved from http://www.sciencedirect.com/science/article/pii/S096999610900309X.
Chagas, M.H., Crippa, J.A., Zuardi, A.W., Hallak, J.E., Machado-de-Sousa, J.P., Hirotsu, C., Maia, L., Tufik, S., and Anderson, M.L. (2013, March). Effects of acute systemic administration of cannabidiol on sleep-wake cycle in rats. Journal of Psychopharmacology, 27(3), 312-6. Retrieved from http://journals.sagepub.com/doi/pdf/10.1177/0269881112474524.
Donat, C.K., Fischer, F., Walter, B., Deuther-Conrado, W., Brodhun, M., Bauer, R.., and Brust, P. (2014). Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet. Acta Neurobiologiae Experimentalis, 74,197-210. Retrieved from http://www.ane.pl/linkout.php?pii=7419.
Fernández-López, D., Lizasoain, I., Moro, M. Á., & Martínez-Orgado, J. (2013). Cannabinoids: Well-Suited Candidates for the Treatment of Perinatal Brain Injury. Brain Sciences, 3(3), 1043–1059. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061885/.
Harvey, B.S., Ohlsson, K.S., Mååg, J.L.V., Musgrave, I.F., and Smid, S.D. (2012, January). Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro. NeuroToxicology, 33(1), 138-146. Retrieved from http://www.sciencedirect.com/science/article/pii/S0161813X11002245.
Mishima, K., Hayakawa, K., Abe, K., Ikeda, T., Egashira, N., Iwasaki, K., and Fujiwara, M. (2005). Cannabidiol Prevents Cerebral Infarction Via a Serotonergic 5-Hydroxytryptamine1A Receptor–Dependent Mechanism. Stroke, 36, 1071-1076. Retrieved from http://stroke.ahajournals.org/content/36/5/1071.long.
López Rodríguez, A.B., Mateos Vicente, B., Romero-Zerbo, S.Y., Rodriguez-Rodriguez, N., Bellini, M.J., Rodriguez de Fonseca, F., Bermudez-Silva, F.J., Azcoitia, I., Garcia-Segura, L.M., and Viveros, M.P. (2011, September). Estradiol decreases cortical reactive astrogliosis after brain injury by a mechanism involving cannabinoid receptors. Cerebral Cortex, 21(9), 2046-55. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bhq277.
Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202.
Nguyen, B.M., Kim, D., Bricker, S., Bongard, F., Neville, A., Putnam, B., Smith J., and Plurad, D. (2014, October). Effect of marijuana use on outcomes in traumatic brain injury. The American Surgeon, 80(10), 979-83. Retrieved from http://www.ingentaconnect.com/content/sesc/tas/2014/00000080/00000010/art00015.
Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V., Kohen, R., Alexandrovich, A., and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease, 22(2), 257-74. Retrieved from http://www.sciencedirect.com/science/article/pii/S0969996105003074.
Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from http://www.nature.com/nature/journal/v413/n6855/full/413527a0.html.
Pazos, M.R., Cinquina, V., Gomez, A., Layunta, R., Santos, M., Fernandez-Ruiz, J., and Martinez-Orgado, J. (2012, October). Cannabidiol administration after hypoxia–ischemia to newborn rats reduces long-term brain injury and restores neurobehavioral function. Neuropharmacology, 63(5), 776-783. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390812002328.
Post-concussion syndrome. (2014, August 19). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/post-concussion-syndrome/basics/definition/con-20032705.
Russo, E.B., Guy, G.W., and Robson, P.J. (2007, August). Cannabis, pain, and sleep: lessons from therapeutic clinical trials of Sativex, a cannabis-based medicine. Chemistry & Biodiversity, 4(8), 1729-43. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200790150/pdf.
Sagredo, O., Pazos, M.R., Satta, V., Ramos, J.A., Pertwee, R.G., and Fernandez-Ruiz, J. (2011, September). Neuroprotective effects of phytocannabinoid-based medicines in experimental models of Huntington’s disease. Journal of Neuroscience Research, 89(9), 1509-18. Retrieved from http://onlinelibrary.wiley.com/wol1/doi/10.1002/jnr.22682/full.
Schurman, L. D., and Lichtman, A. H. (2017). Endocannabinoids: A Promising Impact for Traumatic Brain Injury. Frontiers in Pharmacology, 8, 69. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314139/.
Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., & Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/.
Xu, Z., Lv, X.A., Dai, Q., Ge, Y.Q., and Xu, J. (2016). Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI. Molecular Brain, 9, 75. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971620/.